Archives of Pharmacal Research

, 28:784

Protective effects of EGCG on UVB-induced damage in living skin equivalents

Authors

  • So-Young Kim
    • Department of DermatologySeoul National University College of Medicine
  • Dong-Seok Kim
    • Department of DermatologySeoul National University College of Medicine
    • Research Division for Human Life SciencesSeoul National University
  • Sun-Bang Kwon
    • Welskin Co. Ltd.
  • Eun-Sang Park
    • Department of DermatologySeoul National University College of Medicine
  • Chang-Hun Huh
    • Department of DermatologySeoul National University College of Medicine
  • Sang-Woong Youn
    • Department of DermatologySeoul National University College of Medicine
  • Suk-Wha Kim
    • Department of Plastic and Reconstructive SurgerySeoul National University College of Medicine
    • Department of DermatologySeoul National University College of Medicine
Articles Drug Design

DOI: 10.1007/BF02977343

Cite this article as:
Kim, S., Kim, D., Kwon, S. et al. Arch Pharm Res (2005) 28: 784. doi:10.1007/BF02977343

Abstract

In this study, we evaluate the effects of (−)-epigallocatechin-3-gallate (EGCG) on ultraviolet B (UVB)-irradiated living skin equivalents (LSEs). Histologically, UVB irradiation induced thinning of the LSE epidermis, whereas EGCG treatment led to thickening of the epidermis. Moreover, EGCG treatment protected LSEs against damage and breakdown caused by UVB exposure. Immunohistochemically, UVB-exposed LSEs expressed p53, Fas, and 8-hydroxy-deoxyguanosine (8-OHdG), all of which are associated with apoptosis. However, EGCG treatment reduced the levels of UVB-induced apoptotic markers in the LSEs. In order to determine the signaling pathways induced by UVB, Western blot analysis was performed for both c-Jun NH2-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), which are associated with UVB-induced oxidative stress. UVB activated JNK in the epidermis and dermis of the LSEs, and EGCG treatment reduced the UVB-induced phosphorylation of JNK. In addition, p38 MAPK was also found to have increased in the UVB-exposed LSEs. Also, EGCG reduced levels of the phosphorylation of UVB-induced p38 MAPK. In conclusion, pretreatment with EGCG protects against UVB irradiationvia the suppression of JNK and p38 MAPK activation. Our results suggest that EGCG may be useful in the prevention of UVB-induced human skin damage, and LSEs may constitute a potential substitute for animal and human studies.

Key words

EGCGUVBLiving skin equivalentsApoptosisMAPK
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Copyright information

© The Pharmaceutical Society of Korea 2005